Cardiology Flashcards
Define Stable Angina (Angina pectoris)
Angina refers to classic cardiac pain that is felt when there is a reduction in blood supply to the heart.
Epidemiology of Angina
- Angina is a common presenting complaint, with over 500,000 new cases of angina occurring in the US every year.
- M>F
- More common with increasing age
Risk factors for angina
- Non-modifiable: increasing age, male gender, family history
- Modifiable:hypertension, diabetes, obesity, hypercholesterolaemia, smoking, cocaine use, stress, sedentary lifestyle
Pathophysiology/Aetiology of Angina
Angina is caused by reduced blood flow which causes ischaemia to the heart muscle. This causes severe chest pain.
It usually occurs when the patient has greater than or equal to 70% stenosis.
The small opening that blood flows through might be enough to supply the heart during rest, but if the body demands more blood and oxygen, e.g. during exercise or stressful situations, the heart has to work harder, and therefore needs more blood and oxygen itself.
As the blood flow isn’t meeting the metabolic demands of the heart muscle, patient’s experience symptoms during these times of stress but symptoms are relieved with rest.
Causes:
- In the majority of cases, the underlying cause is atherosclerosis of one or more the coronary arteries.Damage to arterial walls results in inflammation that promotes the formation of atheromatous plaques.Monocytesscavenge lipids upon entry into the arterial wall, transforming into foam cells.Cytokinesare released by foam cells, promotingsmooth muscle migrationfrom the arterial media into the intima. Over time, plaques develop in size.
- Other heart conditions that might lead to stable angina are ones that cause a thickened heart muscle wall e.g. hypertrophic cardiomyopathy. The thicker heart muscles require more oxygen, and if the patients can’t meet increasing demands, they feel pain in the form of angina.
- Aortic stenosis
- Valvular disease
- Arrhythmias
- Embolus to the coronary artery
- Vasculitis: causing aneurysm
- Anaemia: less O2 is transported to the heart
Explain subendocardial ischaemia
This ischaemia is thought to trigger release of adenosine, bradykinin, and other molecules that stimulate nerve fibres in the myocardium that result in the sensation of pain.
This ischaemia is reversible, unlike with myocardial infarction.
Signs of Stable Angina
- Xanthomas or xanthelasma: suggests hypercholesterolaemia
- Hypertension
- A risk factor for angina
- Retinopathy may be seen on fundoscopy
- Evidence of peripheral vascular disease: may coexist with ischaemic heart disease
Symptoms of stable angina
Angina can be precipitated by exertion, heavy meals, cold weather and emotion. Symptoms are usually relieved within 5 minutes by rest or GTN.
- Cardiac-sounding chest pain
- Crushing, left-sided chest pain
- Often radiating to neck, jaw, shoulders and left arm
- Dyspnoea
- Nausea
- Sweating
Physical investigations for angina
heart sounds, signs of heart failure, BMI
First line investigations for angina
12-lead ECG (ST segment depression) and CT angiography (gold standard)
Second line investigations for angina
functional imaging (stress echo, or cardiac MRI) if CT angiography is non-diagnostic
Third line investigations for angina
- transcatheter angiography
Other investigations to consider for angina
- FBC:may reveal anaemia as an underlying cause of angina
- Ambulatory blood pressure monitoring: if hypertension is suspected in clinic
- Fasting blood sugar and HbA1c: diabetes is associated with an increased risk of ischaemic heart disease
- Fasting lipid profile:hyperlipidaemia is associated with an increased risk of ischaemic heart disease
- Thyroid function tests: check for hypo / hyper thyroid
- U&Es: prior to ACEi and other meds
- LFTs: prior to statins
Angina classification
Typical anginausually has all 3 characteristic features listed below, whilstatypical anginahas 2 features andnon-anginal chest painhas 0-1 features.
Characteristic features of angina:
- Discomfort to the chest, neck, jaw, shoulders or arms
- Symptoms brought on by exertion
- Symptoms relieved within 5 minutes by rest or glyceryl trinitrate (GTN)
Symptomatic relief for angina
- GTN spray or tablet: vasodilator
- If pain persists for 5 minutes after the first dose, then repeat the dose. If after 5 minutes the pain still remains, then an ambulance should be called
Anti-anginal medications (1st, 2nd and 3rd line)
1st line: β-blocker OR non-hydropyridine calcium channel blocker
- 2nd line: dual therapy with dihydropyridine calcium channel blocker AND β-blocker
- 3rd line: add additional anti-anginal medication e.g.
- Nitrates
- Ivabradine
- Nicorandil
- Ranolazine
Revascularisation options for angina
- Percutaneous coronary intervention (PCI):aballoon is inflated in a stenosed vessel and a stent is placed to ensure the lumen remains open.
- Coronary artery bypass graft (CABG): involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. Associated with a better overall outcome, however, is associated with greater perioperative risks
Prevention of angina
- Lifestyle changes: exercise, dietary alterations, lipid, diabetes and hypertension management, smoking cessation
- Aspirin and astatin
- Angiotensin-converting enzyme inhibitors(ACEi): if the patient has angina and diabetes
Complications of angina
- MI:a plaque may continue growing until the coronary artery is completely obstructed
- Chronic heart failure:theunderlying causes of ischaemic heart disease are also associated with an increased risk of chronic congestive heart failure
- Stroke:atherosclerosis may also develop within the cerebrovascular system
Prognosis for angina
If lifestyle changes are made and the patient remains compliant with medication, 58% of patients are expected to be free of symptoms.
However, poor lifestyle and poor anti-anginal compliance can predispose a stable atheromatous plaque to become unstable, increasing the risk of myocardial infarction.
Explain the five types of angina
Stable angina: brought on by exertion, relieved by rest
Decubitus angina: induced by lying flat
Unstable angina: occurs on minimal exertion or at rest, with increasing frequency and severity (acute coronary syndrome)
Prinzmetal angina: typically brief chest pain which self-resolves
Nocturnal angina: occurs at night and may wake patient up
Define Acute coronary syndrome
Acute coronary syndrome (ACS) encompasses unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI).
An acute coronary syndrome typically manifests as sudden, new-onset angina, or an increase in the severity of an existing stable angina.
Epidemiology of ACS
- STEMI = 5/1000 per annum in UK
- M>F
Risk factors for ACS
Non-modifiable:
- 65 years or older
- male
- Fx
- Premature menopause
Modifiable:
- Smoking
- DM
- Hyperlipidaemia
- Hypertension
- Obesity
- Sedentary Lifestyle
- Recreational drug use e.g. cocaine
Pathophysiology of ACS
In general, the process underlying all three conditions is atherosclerotic plaque formation.
- Thefirst stageof atherosclerotic plaque formation involves the accumulation of low-density lipoprotein cholesterol in the inner layer of the blood vessel
- Leukocytes adhere to the endotheliumand gain entry into theintima, where they combine with the lipids to becomefoam cells
- Artery remodellingandcalcification, alongside the presence offoam cells, causes atherosclerotic plaques to form
- Rupture of a plaquecauses platelet activation, thrombus formation and coronary artery occlusion. (The thrombus is mainly made up of platelets)
- This results in ischaemia and infarction
In unstable angina and NSTEMI, the occlusion is partial. In STEMI, the occlusion is complete.
In the case of a STEMI, ischaemia is initially just subendocardial, but eventually becomes transmural.
Signs of ACS
- Hypotension or hypertension
- Reduced 4th heart sound
- Signs of heart failure: e.g. increased JVP, oedema; red flag symptom
- Systolic murmur: if mitral regurgitation or a ventricular septal defect develops
Symptoms of ACS
- Chest pain
- Central, ‘heavy’, crushing pain
- Radiation to the left arm or neck
- Symptoms should continue at rest for more than 20 minutes
- Certain patients e.g. diabetics or elderly, have atypical presentation and may not have chest pain (‘silent MI’)
- May sometimes feel like indigestion
- Shortness of breath
- Sweating and clamminess
- Nausea and vomiting
- Palpitations
- Anxiety: often described as a ‘sense of impending doom’
Primary investigations for ACS and findings
ECG:perform within 10 minutes. Aim to perform serial ECGs every 10 minutes to detect dynamic changes.
- Unstable angina: non-specific changes
- NSTEMI: ST-segment depression; T-wave inversion; pathological Q waves; a normal ECG may be seen
- STEMI: ST-segment elevation; T-wave inversion; new left-bundle branch block
Troponin:for a STEMI and NSTEMI, troponin levels will begin to elevate 4-6 hours after injury and will remain elevated for roughly 10 days. In unstable angina, there isnoelevation in troponin.
Other investigations for ACS
- Perform other tests that you would for stable angina e.g.
- Physical Examination (heart sounds, signs of heart failure, BMI)
- Lipid profile
- Thyroid function tests: check for hypo / hyper thyroid
- HbA1C and fasting glucose: check for diabetes
- Coronary angiogram:aim to carry out angiography within 90 minutes if required; diagnostic investigation of choice
- FBC:Hb and haematocrit may reveal a secondary cause in type 2 MI e.g. anaemia
- U&Es:electrolyte imbalances may predispose the patient to cardiac arrhythmias; also done prior to ACEi and other meds
- LFTs: done prior to statins
- Other biomarkers: less commonly used biomarkers of cardiomyocyte injury include creatine kinase-MB (increases at 3-6 hours), andmyoglobin (earliest to rise, usually within 2 hours)
- CXR:to exclude other potential causes, if needed
- Echocardiogram after the event to assess the functional damage
Immediate management for unstable angina and NSTEMI
- Oxygen:only if SpO2is <94%, and aim for 94-98%
- Analgesia:morphine and sublingual glyceryl trinitrate
- Dual antiplatelets:
- Aspirin
- The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance:
- Prasugrel or ticagrelor or clopidogrelif undergoing PCI
- Ticagrelor or clopidogrelif not undergoing PCI
- Anticoagulation:
- Fondaparinux:offer to all patientsunlessundergoing immediate coronary angiography
- Unfractionated heparin:an alternative to fondaparinux if the patient has renal failure
- Beta blockers: e.g. atenolol or metoprolol, unless contraindicated
- Remember ‘MONA’: Morphine,Oxygen,Nitrates,Aspirin
Risk stratification for PCI
If the patient is clinically unstable they must be taken for PCI immediately. Otherwise, the remainder can be risk-stratified using the GRACE score (refer to ‘other notes’ below)
Immediate management for STEMI
- Oxygen:only if SpO2is <94%, and aim for 94-98%
- Analgesia:morphine and sublingual glyceryl trinitrate
- Dual antiplatelets:
- Aspirin
- The choice of the second antiplatelet agent depends on if the person is having PCI or not, and will vary based on local guidance:
- Prasugrel or clopidogrelif undergoing PCI
- Ticagrelor or clopidogrelif undergoing fibrinolysis
Management for STEMI if symptoms onset within 12 hours and access to PCI within 2 hours
- PCI: first-line method of revascularisation; insertion of a catheter via the radial or femoral artery to open up the blocked vessels using an inflated balloon (angioplasty), and a stent may also be inserted
- Anticoagulation and further antiplatelet therapy
- Unfractionated heparinand aglycoprotein IIb/IIIa inhibitor
- Bivalirudinmay be used as an alternative to unfractionated heparin
Management for STEMI is ineligible for PCI
- Thrombolysis e.g. alteplase or tenecteplase
- IV administration of a fibrinolytic agent
- Offered if symptom onset is greater than 12h OR PCI not available within 120 mins
- Anticoagulation
- An antithrombin agent such as unfractionated heparin is usually given alongside thrombolysis
- ECG:if the ECG shows residual ST elevation after 60-90 minutes of thrombolysis, offer immediate angiography and PCI
Secondary prevention for ACS
- Lifestyle changes: exercise, diet change, smoking cessation, reducing alcohol intake
- Manage cardiovascular risk factors: lipid, diabetes, hypertension management
- Antiplatelet therapy:
- Aspirin 75mg OD continued indefinitely
- The second antiplatelet depends on the one chosen in the acute setting i.e. prasugrel, ticagrelor, or clopidogrel, and is usually continued for 12 months.
- Angiotensin-converting enzyme inhibitors(ACEi) andbeta-blocker
- Statin:usually atorvastatin 80mg
- Cardiac rehabilitation: must be offered following myocardial infarction
Early complications of ACS
- Post-MI pericarditis:inflammation of the pericardium usually occurs afew dayspost-MI due to irritation of the pericardium; usually benign
- Cardiac arrest/tachyarrhythmias:most commonlydue to ventricular fibrillation
- Can lead to sudden death
- Bradyarrhythmias:heart block is more common after an inferior myocardial infarction
- Cardiogenic shock:extensive ventricular damage may lead to impaired ejection fraction and the development of cardiogenic shock
- Ventricular septal defect:seen within the first week and may present with acute heart failureand a pansystolic murmur
- Mitral regurgitation:most commonly due topapillary muscle rupture secondary to an inferior-posterior infarction, results in an early-mid systolic murmur
- Left ventricular wall rupture: a rare but fatal complication which presents within a few weeks. Ischaemia leads to a weakened ventricular wall and rupture, presenting as cardiac tamponade and acute heart failure
Late complications of ACS
- Dressler’s syndrome:presents similarly to post-MI pericarditis but occurs2-6 weekspost-MI, and reflects anautoimmuneprocess against neo-antigens formed by the heartDiagnosis:ECG(global ST elevationandT wave inversion),echocardiogram (pericardial effusion) and raisedinflammatory markers(CRPandESR).Management:NSAIDs(aspirin/ibuprofen) and in more severe cases steroids (prednisolone). May needpericardiocentesisto remove fluid around the heart.
- Heart failure:ventricular dysfunction following extensive damage can lead to chronic heart failure
- Left ventricular aneurysm: bulge or ballooning of a weakened area of the heart
Prognosis for ACS
Unstable anginahas a better outcome than anNSTEMIorSTEMI.
NSTEMIs and STEMIs have similar long-term outcomes. 5-10% of patients with ACS are predisposed tore-infarction.
Poor prognostic factorsinclude: increasing age, the magnitude of troponin rise, arrhythmias, left ventricular dysfunction,renal impairment, diabetes, anaemia, cerebrovascular disease
Types of MI
- Type 1: a classic MI and occurs due to atheromatous plaque rupture
- Type 2: secondary to ischaemia due toeitherincreased oxygen demandordecreased supply, such as vasospasm, anaemia and sepsis. Management involves treating the underlying cause.
- Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
- Type 4: MI associated with PCI / coronary stenting / CABG
ACS medications
Aspirin - Antiplatelet: predominantly COX-1 inhibition, thus preventing the synthesis of thromboxane A2
Clopidogrel, Prasugrel and Ticagrelor - Antiplatelets: inhibit the binding of ADP to its platelet P2Y12 receptor
Tirofiban, Abciximab, eptifibatide - Antiplatelets: glycoprotein IIb/IIIa receptor antagonists
Enoxaparin, Fondaparinux - Anticoagulants: activate antithrombin III, thus causing the inhibition of clotting factor Xa
Bivalirudin - Anticoagulant: reversible direct thrombin inhibitor
GRACE score for ACS
The Global Registry of Acute Coronary Events (GRACE) score is recommended by NICE to risk-stratify patients with unstable angina and non-ST elevation myocardial infarction (NSTEMI).
The GRACE score estimates admission to 6-month mortality.
Variables: Age, HR, Pulse, Systolic BP, Creatinine, Cardiac arrest at admission, ST-segment deviation on ECG, Abnormal cardiac enzymes, Kilip class (Signs/symptoms) - Rales and/or jugular venous distension, Pul oed, CArdiogenic shock
Interpretations:
Intermediate- and high-risk patients with unstable angina or NSTEMIrequire coronary angiography during admission, whilst this can be delayed in low-risk patients.
- Clinically unstable:immediate angiogram and percutaneous coronary intervention (PCI)
- Intermediate or high risk of cardiovascular event (>3%):coronary angiography and percutaneous coronary intervention (PCI) within 72 hours of admission
- Low risk of cardiovascular event (<3%):exclusively medical management
Define congestive heart failure
Cardiac failure describes when cardiac output cannot meet metabolic demands.
Congestive cardiac failure describes a combination of left and right-sided ventricular failure.
Epidemiology of congestive heart failure
- M>F
- More prevalent with increasing age
Risk factors for congestive heart failure
- Previous myocardial infarction:the single greatest risk factor
- Non-modifiable risk factors: male gender, increasing age
- Cardiovascular risk factors: ischaemic heart disease, hypertension, hypercholesterolaemia, diabetes
- Valvular heart disease
- Renal failure: causes ‘high-output’ heart failure due to fluid overload
- Atrial fibrillation
Aetiology of congestive heart failure
In heart failure, cardiac output struggles to meet the metabolic demands of the body.
Heart failure can happen one of two ways: systolic failure or diastolic failure:
- Systolic heart failure
- Cardiac output = stroke volume x heart rate
- The ejection fraction is not preserved: an ejection fraction of 40% or less would indicate systolic heart failure.
- The low stroke volume is due to the ventricles not pumping enough blood out.
Diastolic:
- Cardiac output = stroke volume x heart rate
- In this case, the stroke volume is low but the ejection fraction is preserved. The reason for the low stroke volume is due to reduced filling of the ventricle (reduced preload)
Congestive cardiac failure describes a combination of left and right-sided ventricular failure (biventricular failure). Right-sided heart failure usually occurs as a result of left-sided heart failure. Blood starts backing up into the lungs causing pulmonary oedema and congestion. The pulmonary hypertension puts pressure on the right ventricle (cor pulmonale) and causes right-sided heart failure. The pulmonary congestion is responsible for the respiratory symptoms seen in heart failure.
Causes of systolic failure
- Ischaemic heart disease: as less blood and oxygen get to the myocardium, the myocytes start to die
- Hypertension: as arterial pressure increases in the systemic circulation, it gets harder for the left ventricle to pump blood out into that hypertensive systemic circulation.
- Left ventricular hypertrophy: increased muscle mass requires increased oxygen supply - making it more likely for that the muscle will die
- Dilated cardiomyopathy: heart chambers dilate and thin out, leading to weaker contractions.
Causes of diastolic failure
- Left ventricular hypertrophy: causes the ventricular chamber to decrease in size which means less blood can enter.
- Restrictive cardiomyopathy: ventricle can’t stretch enough to accommodate the blood
- Valvular disease: e.g. aortic stenosis causes LVH or mitral regurgitation means blood doesn’t enter the ventricles in the right amount as it leaks back into atria
- Arrhythmias e.g. atrial fibrillation
Pathophysiology of congestive heart failure
- In anormalheart, increased ventricular filling results in increased contraction via theFrank-Starling law→ increased cardiac output
- In patients with heart failure, this mechanismfails
- As the heart continues to fail →compensatory mechanismsare activated, including anincrease in heart rate,catecholamine releaseandRAAS activation (due to decreased blood flow to kidneys)
- These mechanisms are useful in theinitialperiod but are usuallyoverexpressed, thus instigating avicious cycle.
- Compensatory mechanisms are usually responsible for the fluid retention and fluid overload symptoms experienced by the patient
Signs of left sided heart failure
- Tachypnoea and tachycardia
- Cool peripheries
- Peripheral or central cyanosis
- Displaced apex beat
- Stony dull percussion: if an effusion is present
- Crackles on auscultation: coarse bi-basal crackles due to pulmonary congestion
- Third heart sound (S3)
Symptoms of left sided heart failurw
- Dyspnoea: particularly exertional
- Orthopnoea (SOB when lying flat) and paroxysmal nocturnal dyspnoea (SOB at night)
- Fatigue and weakness
- Cough with pink, frothy sputum
- Cardiogenic wheeze
Signs of right sided heart failure
- Due to backing up of fluid:
- Raised JVP
- Peripheral pitting oedema
- Hepatosplenomegaly
- Ascites
Symptoms of Right sided heart failure
- Fatigue and weakness
- Due to backing up of fluid
- Swelling in the legs
- Distended abdomen
Severity criteria for congestive heart failure
Class I: no limitation on physical activity, ordinary activity doesn’t cause fatigue, palpitations or dyspnoea
Class II: slight limitation on physical activity, comfortable at rest but physical activity causes symptoms
Class III: Marked limitation of physical activity, comfy at rest but not physical activity
Class IV: Cant carry out physical activity without discomfort, symptoms of cardiac insufficiency at rest
Primary investigations for congestive heart failure
- NT-proBNP: increased in chronic heart failure
- ECG:broad QRS complexes; evidence of left ventricular hypertrophy
- CXR:
- A-Alveolar oedema (batwing opacities)
- B- KerleyBlines
- C-Cardiomegaly
- D-Dilated upper lobe vessels
- E- Pleural effusion
- Transthoracic echocardiogram:determine left ventricular ejection fraction (LVEF), diastolic function, and valvular abnormalities
Other investigations to consider for congestive heart failure
- FBC:anaemia may be a cause of ‘high-output’ heart failure
- U&Es: to investigate for renal failure as an underlying cause of heart failure; also U&Es monitored as ACEi’s and aldosterone antagonists can cause electrolyte abnormalities
- Blood lipids and fasting blood glucose:screen for hypercholesterolaemia and evidence of diabetes
1st line management for congestive heart failure
- Beta-blocker e.g. bisoprolol and ACE inhibitor e.g. ramipril: start one drug at a time.
- Beta-blockers and ACE inhibitors shown to improve mortality but not in heart failure withpreservedejection fraction
- If ACE inhibitor is not tolerated: angiotensin receptor blocker (e.g losartan) or hydralazine with nitrate (particularly in Afro-Caribbean patients)
2nd line management for congestive heart failure
Aldosterone antagonist (e.g. spironolactone) if symptoms not controlled with 1st line management
3rd line management for congestive heart failure
- Cardiac resynchronisation therapy(CRT): involves biventricular pacing and forces both ventricles to contract in synchrony, thereby improving cardiac outputOR
- Implantable cardioverter-defibrillator (ICD): able to perform cardioversion, defibrillation and, in some cases, pacing
- Digoxin: an alternative option, particularly for patients with AFand heart failure due to its inotropic effects.
- Ivabradine: an alternative option ifHR >75 bpmandLVEF <35%; slows the heart rate so the heart can pump more blood through the body each time it beats.
Other management for congestive heart failure
- Smoking cessation, diet changes, exercise
- Fluid restriction: usually limited to <1.5L/day
- Loop diuretic(e.g. furosemide): symptomatic relief of fluid overload
- Annual influenza vaccineandone-off pneumococcal vaccine
- Sacubitril-valsartan(Entresto): consider if the patient is symptomatic on an ACE inhibitor or ARBANDhas a reduced LVEF; works by relaxing blood vessels so that blood can flow more easily, making it easier for heart to pump blood.
- Surgical replacement of valve if valvular disease
- Cardiac transplantation: considered for patients with severe refractory symptoms or refractory cardiogenic shock
Complications of congestive heart failure
- Pleural effusion:heart failure causes an elevated pulmonary capillary pressure, usually resulting in bilateral transudative pleural effusions
- Acute decompensation of chronic heart failure:patients usually present with acute respiratory distress due to significant pulmonary oedema
- Arrhythmias
- Acute renal failure:reduced cardiac output and drug overuse (ACE inhibitors, aldosterone antagonists, diuretics) results in poor renal perfusion
Prognosis for congestive heart failure
In general, the survival of patients with end-stage heart failure is poor. For example, 65% of patients in NYHA class IV are alive at 17-month follow-up.
Define acute decompensated heart failure
Cardiac output is not able to meet metabolic demands. This can be new-onset or as an acute decompensation of chronic heart failure.
Epidemiology of acute decompensated heart failure
- In the UK, heart failure is responsible for over 67,000 hospital admissions per year
- > 65 years of age
Risk factors for acute decompensated heart failure
Increasing age
Coronary artery disease
Hypertension
Valvular disease
Diabetes
A Fib
Renal insufficiency
Pathophysiology/Aetiology of acute decompensated heart failure
Acute decompensated heart failure can occur as either new-onset heart failure without any previous cardiac dysfunction or as an acute decompensation of chronic heart failure.
In heart failure, cardiac output is not able to meet the metabolic demands of the body.
Common causes of heart failure include coronary artery disease and hypertension.
General pathophysiology:
- In response to reduced cardiac output, thesympathetic nervous systemis activated
- This results intachycardia, increasedmyocardial contractility, peripheralvasoconstriction, andRAASactivation, causing salt and water retention
- Patients with heart failure are generally hypervolemic → brain natriuretic peptide (BNP) release by ventricular myocytes in response to stretch
- These processes lead topulmonary and/or venous congestion
- Pulmonary oedemapresents with shortness of breath, whilst venous congestion causesperipheral oedema
Signs of acute decompensated heart failure
- Cool peripheries
- Signs of congestive heart failure: peripheral, pitting oedema and raised JVP
- Displaced apex beat
- Hypotension
- Crackles on auscultation: left-sided failure; usually coarse bi-basal crackles
- Third heart sound (S3)
- Stony dull percussion: if an effusion is present
Symptoms of acute decompensated heart failure
- Dyspnoea: due to pulmonary oedema
- Often a history of orthopnea and paroxysmal nocturnal dyspnoea
- Fatigue and weakness
- Cardiogenic wheeze
- Symptoms of congestive heart failure: swelling of the peripheries and ascites
Investigations for acute decompensated heart failure
- FBC:anaemia can be an underlying cause of heart failure
- U&Es: to investigate renal failureas an underlying cause of heart failure. Renal function should be monitored because loop diuretics such as furosemide are nephrotoxic.
- Arterial blood gas: demonstrates type 1 respiratory failure; degree of acidosis helps to determine which patients may require non-invasive ventilation
- BNP or NT-proBNP:BNP <100 pg/ml or NT‑proBNP <300 pg/ml suggest an alternative diagnosis
- ECG: may be AF; left ventricular hypertrophy
- CXR: pulmonary congestion features include:
- A-Alveolar oedema (batwing opacities)
- B- KerleyBlines
- C-Cardiomegaly
- D -Dilated upper lobe vessels
- E- PleuralEffusion
- Transthoracic echocardiogram:assess for systolic and diastolic function, ejection fraction and valvular disease (NICE defines a reduced left ventricular ejection fraction as < 40%)
Acute management for Acute decompensated heart failure
- Stabilise the patient: administer oxygen to maintain a SpO2≥94%
- Fluid restriction: fluid intake is usually limited to <1.5L/day
- IV diuretic: usually a loop diuretic e.g. furosemide to relieve fluid overload
- Inotropes or vasopressors e.g. dobutamine: only offer to patients with heart failure and cardiogenic shock (i.e. haemodynamically unstable)
- Non-invasive ventilation (NIV): consider NIV if the patient does not stabilise with initial medical management
- Continuous positive airway pressure (CPAP)
- Intubation and ventilation: if CPAP is unsuccessful
Surgical management for acute decompensated heart failure
- If acute heart failure is due to aortic stenosis: offersurgical aortic valve replacement
- Mechanical assist device: pump that can temporarily help the pumping action of the heart
Long term management for acute decompensated heart failure
- ACE-inhibitor e.g. ramiprilanda cardioselective β-blocker e.g. bisoprolol
- Improved prognosisby slowing, or even reversing, ventricular remodelling
- Fluid restriction: fluid intake is usually limited to <1.5L/day
- Loop diuretic (e.g. furosemide) forsymptomaticrelief of oedema
Complications of acute decompensated heart failure
Arrhythmias: can both precipitate acute heart failure and occur as a result of it. Atrial fibrillation is one of the most common arrhythmias associated with heart failure.
Prognosis for acute decompensated heart failure
Mortality for acute heart failure ranges from 2-20%.
Poor prognostic factors include old age, hypotension, male sex, ischaemic congestive heart failure, renal dysfunction, previous chronic heart failure, a respiratory rate on admission > 30 and an elevated BNP.
Define Hypertension
Hypertension refers to a persistent elevation of arterial blood pressure.
Hypertension is defined as a blood pressure reading of ≥140/90 mmHg (ambulatory blood pressure monitoring ≥135/85 mmHg) and is categorised into primary or secondary hypertension, depending on whether a cause can be identified.
Normal blood pressure = 120/80 mmHg
Epidemiology of hypertension
- Hypertension is responsible for 7.5 million deaths annually and is a major contributor to ischaemic heart disease
- M>F
- Prevalence is in those older than 35
Risk factors for hypertension
- Non-modifiable risk factors: increasing age, African heritage, family history
- Modifiable risk factors: obesity, sedentary lifestyle, alcohol excess, smoking, high sodium intake (>1.5g/day), stress
Pathophysiology/aetiology of hypertension
Any changes in blood pressure, and consequently the development of hypertension, occur due to alterations in cardiac output and peripheral resistance.
- Primary (essential) hypertension: has no known underlying cause and is responsible for 90-95% of cases of hypertension. Some contributing factors include:
- Genetic susceptibility
- Excessive sympathetic nervous system activity
- Abnormalities of Na+/K+ membrane transport
- High salt intake
- Abnormalities in renin-angiotensin-aldosterone system
- Secondary hypertensionindicates a known underlying cause. Examples include:
- Renal disease: glomerulonephritis, polycystic kidney disease, renal artery stenosis, chronic kidney disease
- Endocrine disorders: primary hyperaldosteronism, phaeochromocytoma, Cushing’s syndrome, hyperthyroidism, acromegaly
- Medication:glucocorticoids, ciclosporin, atypical antipsychotics, the combined oral contraceptive pill
- Pregnancy (pre-eclampsia)
Stages and subtypes of Hypertension
Stage 1: 140/90 or above
Stage 2: 160/100 or above
Stage 3: 180/120 or above
- White-coat effect: a discrepancy of ≥20/10mmHg between the clinic reading and average daytime ABPM reading suggests ‘white-coat’ hypertension
- Malignant (accelerated) hypertension: a severe increase in blood pressure ≥180/120 mmHg with signs of retinal haemorrhage and/or papilloedema, associated with target organ damage. These patients require emergency assessment!
Signs of hypertension
- Malignant (accelerated) hypertension (≥180/120 mmHg):
- Hypertensive retinopathy
- Visual disturbance
- Cardiac symptoms e.g. chest pain
- Oliguria or polyuria
- Secondary hypertension: signs of the underlying cause e.g. hyperthyroidism causes weight loss, sweating and palpitations
Symptoms of hypertension
- Asymptomatic: most common presentation
- Headaches: classically occipital and worse in the morning
- Dizziness, Blurred vision
Describe blood pressure findings for hypertension
- Blood-pressure reading:record the blood pressure on both arms
- If the clinic blood pressure is ≥140/90mmHg, take asecond reading. Record thelowerof the 2 measurements as the clinic blood pressure
- If the difference in blood pressurebetween armsis > 20mmHg, repeat the measurements. If readings remain > 20 mmHg, then subsequent measurements should be from the arm with thehigher reading
Describe ambulatory blood pressure monitoring
- Offer to all patients with a clinic blood pressure between 140/90 mmHg and 180/120 mmHg to confirm the diagnosis
- Blood pressure is measured over a 24 hour period, with at least2 measurements per hourduring waking hours
- An overall of at least 14 measurements are required
Explain home blood pressure monitoring
- Offered if ABPM is not appropriate; HPBM involves the patient checking their blood pressure manually throughout the day
- With the patient seated for each reading, two consecutive measurements are requiredat least 1 minute apart
- Blood pressure should be measuredtwice daily, usually in the morning and evening, and ideally recorded for 7 days butat least4 days
- Readings on the first day are discarded and the average of the remaining readings are used
Other investigations for hypertension
- Fundoscopy: assess for hypertensive retinopathy
- 12-lead ECG: assess for ischaemic changes and evidence of left ventricular hypertrophy
- Albumin:creatinine ratio (ACR) and urinalysis: assessing for renal dysfunction, as evidenced by elevated ACR and proteinuria or haematuria on urinalysis
- Bloods: HbA1c, U&Es, total cholesterol and HDL cholesterol
- It is also important to formally estimate cardiovascular risk using a tool such as QRisk to discuss prognosis and healthcare options.
Other investigations for hypertension
- Fundoscopy: assess for hypertensive retinopathy
- 12-lead ECG: assess for ischaemic changes and evidence of left ventricular hypertrophy
- Albumin:creatinine ratio (ACR) and urinalysis: assessing for renal dysfunction, as evidenced by elevated ACR and proteinuria or haematuria on urinalysis
- Bloods: HbA1c, U&Es, total cholesterol and HDL cholesterol
- It is also important to formally estimate cardiovascular risk using a tool such as QRisk to discuss prognosis and healthcare options.
Diagnostic criteria for hypertension
Hypertension is confirmed when the following criteria are met:
- Clinic blood pressure of 140/90 mmHg or higherand
- ABPM daytime average or HBPM average of 135/85 mmHg or higher
Treatment targets for hypertension
- <80 years: <140 systolic; <90 diastolic
- > 80 years: <150 systolic; <90 diastolic
First and second line management for hypertension
First line: prevention and lifestyle change (e.g. diet, exercise and weight loss)
Second line: ACE-i
3rd line for management for hypertension
Triple therapy: combine ACEi (or ARB) with CCB (amlodipine) and thiazide-like diuretic (indapamide)
4th line management for hypertension
Quadruple therapy: dependant on potassium levels. If hypertension is not controlled with 4 drugs, then consider a specialist review.
- IfK+ >4.5, add an alpha- or beta-blocker
- IfK+ ≤4.5, add an aldosterone antagonist such as spironolactone (a ‘K+ sparing diuretic’)
Other treatment options for hypertension
- Direct renin inhibitors e.g. aliskiren: a new option
- Block the conversion of angiotensinogen to angiotensin I
- Generally only considered in patientsintolerantto normal antihypertensives
Monitoring for hypertension
NICE recommend measuring blood pressure every 5 years to screen for hypertension. It should be measured more often in patients that are on the borderline for diagnosis (140/90) and every year in patients with type 2 diabetes.
Complications of hypertension
- Coronary artery disease:for every 20/10 mmHg increase in blood pressure, there is a doubling of mortality related to ischaemic heart disease
- Cerebrovascular accident:linear association between increased blood pressure and risk of developing a cerebrovascular accident
- Congestive heart failure:hypertensive patients are 3 times more likely to develop congestive heart failure
- Chronic kidney disease:increased levels of blood pressure are associated with the development of renal disease
- Hypertensive retinopathy
Prognosis for hypertension
Maintaining a tight control on blood pressure reduces the risk of developing end-organ damage, as well as cardiovascular and cerebrovascular disease, thus reducing the overall morbidity and mortality rate associated with hypertension.
Define Arrhythmia
Arrhythmias are abnormal heart rhythms. They result from an interruption to the normal electrical signals that coordinate the contraction of the heart muscle.
Explain the four cardiac arrest rhythms
These are the four possible rhythms that you will see in a pulseless unresponsive patient.
Shockable rhythms:
- Ventricular tachycardia
- Ventricular fibrillation
Non-shockable rhythms:
- Pulseless electrical activity(all electrical activity except VF/VT, including sinus rhythm without a pulse)
- Asystole(no significant electrical activity)
Define Atrial fibrillation (AF)
Atrial fibrillation (AF) is a chaotic irregular atrial arrhythmia and is considered a type of supraventricular tachycardia (SVT)
Epidemiology of AF
- Atrial fibrillation is the most common cardiac arrhythmia and is estimated to affect approximately 2.5% of the general population
- More common with increasing age
- M>F
Risk factors for AF
- Increasing age: AF affects approximately 5% of patients aged 70-75 years, and 10% of patients aged 80-85 years
- Diabetes mellitus
- Hyperthyroidism
- Hypertension
- Congestive heart failure
- Valvular heart disease
- Coronary artery disease
- Dietary and lifestyle factors: excessive caffeine intake, alcohol abuse, obesity, smoking, medication use (e.g. thyroxine or beta-agonists)
Pathophysiology/Aetiology of AF
Normally, the sinoatrial node produces organised electrical activity that coordinates the contraction of the atria of the heart. Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregular. This is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.
This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles. This results in:
- Irregularly irregularventricular contractions
- Tachycardia
- Heart failuredue topoor fillingof the ventricles duringdiastole
- Risk ofstroke
Types of AF
- First episode
- Paroxysmal: recurrent episodes that stop on their own in less than 7 days
- Persistent: recurrent episodes that last more than 7 days
- Permanent: continuous atrial fibrillation that is also refractory to treatment. Management is aimed at rate control and anticoagulation, if appropriate.
Acronym for AF causes
PIRATES
P - Pulmonary Embolism or COPD
I - Ischaemic Heart Disease
R - Rheumatic heart disease
A - Anaemia, Age and Alcohol
T - Thyroid disease
E - Electrolyte disturbance
S - Sepsis and Sleep apnoea
Signs of AF
- Irregular irregular pulse
- Hypotension:red flag; suggest haemodynamic instability
- Evidence of heart failure:red flag; such as pulmonary oedema
Symptoms of AF
- Palpitations
- Dyspnoea
- Chest pain: red flag
- Syncope: red flag
Adverse features of AF
The presence of adverse features guides the decision to undergo DC cardioversion.
- Shock: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
- Syncope: transient loss of consciousness
- Myocardial ischaemia: typical ischaemic chest pain and/or evidence of myocardial ischaemia on 12-lead ECG
- Heart failure: pulmonary oedema and/or raised jugular venous pressure
Primary Investigations for AF
- ECG:irregularly irregular QRS complexes with absent P waves and chaotic baseline
- 24-hour ambulatory ECG monitoring is recommended for those with paroxysmal AF in the community
- Serum electrolytes:in addition to standard electrolytes, magnesium, calcium and phosphate should also be assessed
- TFTs: hyperthyroidism is a secondary cause of AF
Other investigations for AF
- Cardiac biomarkers:request troponin if chest pain is present as this may reflect an MI
- Chest x-ray:if there is suspicion of heart failureto assess for pulmonary oedema
- Transthoracic ECHO:consider if there is a suspicion of underlying structural or functional heart disease; usually performed prior to cardioversion in chronic cases
Overview of Management of AF
- Determine if rate control or rhythm control is more appropriate:
- Rate controlaccepts the fact that the patient is not in sinus rhythm, but the aim is to get the heart rate below 100 to extend the time during diastole when the ventricles can fill with blood.
- Rhythm controlaims to restore normal sinus rhythm and is known as ‘cardioversion’, can either be electrical or pharmacological
Management for AF if haemodynamically unstable
Emergency electrical synchronised DC cardioversion
Management for AF if haemodynamically stable
- Onset of AF < 48 hours: 1) rate control or 2) rhythm-control
- Onset of AF > 48 hours / unknown onset: offer rate-control and anticoagulation for at least 3 weeks, then offer rhythm control if appropriate e.g. if rate control is unsuccessful or the patient remains symptomatic
Explain rate control for AF
- First line: beta-blocker(e.g. bisoprolol) or arate-limiting calcium-channel blocker (e.g. verapamil)
- Digoxin: may be considered first-line in patients with AF and heart failure
- Second line: if refractory then consider combination therapy
Explain rhythm control for AF
- Pharmacological:
- Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease
- Amiodarone: if structural/ischaemic heart disease is present
- Electrical cardioversion:rapidly shock the heart back into sinus rhythm
What to do if AF fails
Left atrial ablation: thepulmonary veinssupply the premature depolarisations that trigger AF; radiofrequency energy is delivered in this area
When to refer to cardiology for AF
Required if:
- Rhythm control is appropriate
- Rate-control treatment fails to control the symptoms of AF
- The person is found to havevalvular disease or left ventricular systolic dysfunctionon echocardiography
- Wolff–Parkinson–White syndrome or a prolonged QT intervalis suggested by electrocardiogram
Stroke prevention for AF
Anticoagulation: to reduce risk of thromboembolism
Complications for AF
- Stroke:blood can pool within the atria, increasing the risk of thromboemboli and subsequent ischaemic stroke
- Myocardial infarction:sustained. tachycardia in patients with coronary artery disease can result in acute myocardial infarction
- Heart failure: sustained tachycardia in patients with other cardiac co-morbidities can result in myocardial ischaemia and a reduced ejection fraction
- Reduced quality of life
Prognosis for AF
The prognosis is ultimately determined by the presence of an underlying condition that may be potentially reversible, such as sepsis or hyperthyroidism.
Overall, AF is associated with an increased mortality rate since it acts as an independent risk factor for stroke and myocardial infarction.
Review any person with an established AF diagnosis at least annually.
Explain CHA2DS2-VASc score
CHA2DS2-VASc used to calculate stroke risk when considering anticoagulation
C - Congestive heart failure
H - Hypertension
A2 - Age 65-74 or 75+
D - Diabetes
S2 - Stroke/TIA/thromboembolism history
V - Vascular disease
S - Female sex
If score 2 then give blood thinner
HAS-BLED score
HAS-BLED estimates the risk of major bleeding for patients on anticoagulation to assess risk-benefit in AF care
H - Hypertension
A - Abnormal renal or liver function
S - Stroke history
B - Bleeding history
L - Labile INR
E - Elderly
D - Drugs NSAID’s e.g. clopidogrel, aspirin, NSAID
Above 4 is high risk
Define Atrial flutter
Atrial flutter is usually an organised atrial rhythm with an atrial rate typically between 250-350bpm
Epidemiology of Atrial flutter
- Much less common than AF
- M>F
- Prevalence increases with age
Aetiology of Atrial flutter
- Idiopathic (30%)
- Coronary heart disease
- Obesity
- Hypertension
- Cardiomyopathy
- Heart failure
- Thyrotoxicosis
- COPD
- Pericarditis
- Acute excess alcohol intoxication
Pathophysiology of Atrial flutter
Normally the electrical signal passes through the atria once, simulating a contraction then disappears through the AV node into the ventricles.
Atrial flutter is caused by a “re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway. The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm.
The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction.
Can be paroxysmal or persistent.
Clinical manifestations of Atrial flutter
- Palpitations
- Breathlessness
- Chest pain
- Dizziness
- Syncope
- Fatigue
Investigations for Atrial flutter
ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave
Management for Atrial flutter
- Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
- Rate/rhythm controlwith beta blockers or cardioversion
- Radiofrequency ablationof the re-entrant rhythm
- Anticoagulationbased on CHA2DS2VASc score
Define Bradycardia
Bradycardia is defined as a heart rate below 50 beats per minute, which can either be physiological or due to sinus node or atrioventricular (AV) node conduction dysfunction.
Epidemiology of Atrial flutter
The incidence of AV conduction abnormalities increases with age, corresponding with the age-related incidence of ischaemic heart disease.
Risk factors for Atrial flutter
- Increasing age (> 70 years old): increases the risk of sinoatrial and AV node dysfunction
- Endocrine:hypothyroidism
- Infections: e.g. typhoid and diptheria
- Electrolytes: hyperkalaemia, hypokalaemia, hypercalcaemia, or hypocalcaemia
- Cardiac: recent MI
- Drugs: e.g. beta-blockers, non-dihydropyridine calcium channel blockers, digoxin, adenosine and amiodarone
- Surgery: intra-operative sinus bradycardia is relatively common
- Hypothermia
Pathophysiology of Bradycardia
Sinus node dysfunction may be associated with sinus bradycardia, tachycardia-bradycardia, and sick sinus syndrome.
Atrioventricular(AV) conduction disturbances can either be due to poor transmission of atrial depolarisation to the ventricles or a delay in atrial depolarisation.
Types of AV blocks:
First-degree AV block: occurs where there is delayed atrioventricular conduction through the AV node but every atrial impulse leads to a ventricular contraction.
Second-degree AV block(failure of conduction from atria to ventricles):
- Mobitz type I / Wenckebach: atrial inputs becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong.
- Mobitz type II: Usually due to disease of the His-Purkinje system which causes intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes.
Third-degree AV block: complete heart block. This is no observable relationship between P waves and QRS complexes.
Signs of Bradycardia
- Associated with Cushing’s triad:raised intracranial pressure
- Bradycardia
- Hypertension
- Irregular respirations (apnoea)
- JVP:cannon A waves
- Occurs in complete heart block due to atrial contraction against a closed tricuspid valve
Symptoms of Atrial flutter
- Dizziness
- Fatigue
- Shortness of breath
- Syncope
Primary investigations for atrial flutter
ECG
- First-degree AV block: PR interval >0.2s
- Mobitz type I / Wenckebach: increasing PR interval culminating in a dropped QRS complex. The PR interval resets and the cycle repeats.
- Mobitz type II: the PR interval remains constant, but with intermittent dropped QRS complexes (2:1, 3:1, etc).
- Third-degree AV block: P wave and QRS complex are completely dissociated
Other investigations for atrial flutter
- TFTs:hypothyroidism may be responsible for the bradycardia
- U&Es and metabolic panel: screen forhyperkalaemia, hypokalaemia, hypercalcaemia, or hypocalcaemia
- Serum digoxin level: appropriate for patients on digoxin
- Holter monitoring: allows the correlation of symptoms with episodes of bradycardia
- Tilt-table testing: to assess forneurocardiogenicsyncope, whereby head-upright tilting causes a sudden drop in blood pressure followed by bradycardia
- ECHO: useful if a permanent pacemaker is being implanted in order to assess left ventricular ejection fraction (LVEF)
- LVEF<30%would warrant a pacemakerandan implantable cardioverter-defibrillator
Management of bradycardia for stable, unstable and high risk of asystole patients
- If stable: observe
- If unstable or risk of asystole
- First line: atropine500mcg IV
- If no improvement:
- Atropine500mcg IV repeated
- Otherinotropes(such as noradrenalin)
- Transcutaneous cardiac pacing(using a defibrillator)
- In patients with high risk ofasystole
- Temporary transvenous cardiac pacingusing an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
- Permanent implantable pacemakerwhen available
Complications of bradycardia
- Syncope
- Arrhythmias:some patients may go on to develop asystole, ventricular tachycardia or ventricular fibrillation
- Congestive heart failure: due to poor cardiac output
Prognosis for Bradycardia
Bradycardia treated with a pacemaker will typically have a good prognosis.
Pathophysiology of RBBB
- Right bundle branch block (RBBB):
- Causes: pulmonary embolism, cor pulmonale, ischaemic heart disease, atrial/ ventricular septal defect
- Right bundle no longer conducts, meaning that the two ventricles do not get impulses at the same time. The impulse therefore spreads from left to right, which produces late activation of right ventricle.
Pathophysiology of LBBB
- Causes: ischaemic heart disease, hypertension, cardiomyopathy, idiopathic fibrosis
- Results in late activation of left ventricle
- As the left bundle branch conduction is normally responsible for the initial ventricular activation, left bundle branch block also produce abnormal Q waves
- Bifascicular block: blockage of right bundle branch and left anterior fascicle
- Complete block: failure of all bundle branches
Clinical manifestations of RBBB and LBBB
- Usually asymptomatic
- RBBB: wide physiological splitting of second heart sound
- LBBB: reverse splitting of the second heart sound
ECG for LBBB and RBBB
- RBBB:
- Wide, slurred S wave in V6 and as a tall late R wave in V1
- MarroW: QRS looks like an M in V1, QRS looks like a W in V5 and V6
- LBBB:
- Deep S wave in V1 and a tall late R wave in V6
- WilliaM: QRS looks like a W in V1 and V2, QRS looks like an M in V4-V6
Define Sinus tachycardia
Under normal circumstances at rest, our heart should be in sinus rhythm with an accompanying rate of 60-100 bpm. If the defining features of normal sinus rhythm are met but the heart rate is fast (> 100 bpm), we call it sinus tachycardia.
Aetiology of sinus tachycardia
- Anxiety
- Exercise
- Pain
- Anaemia
- Haemorrhage
- Thyrotoxicosis
- Heart failure
- Pulmonary embolism
Investigations for sinus tachycardia
ECG: one P wave per QRS, constant PR interval
Management for Sinus tachycardia
- Treat underlying cause
- Beta blockers may be used
Define Supraventricular tachycardia (SVT)
Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles
Epidemiology of SVT
- The incidence of paroxysmal SVT is 1-3 cases per 1000 persons, with a prevalence of 0.2%
- Elderly females are the most commonly affected group
Risk factors for SVT
- Increasing age: five times more common in elderly patients
- Female gender: two times more common in females
- Hyperthyroidism
- Smoking
- Excessive caffeine or alcohol consumption
- Stress: physical or emotional stress
- Medication: e.g. salbutamol, atropine, decongestants (e.g. pseudoephedrine)
- Recreational drug use: cocaine and methamphetamines
Pathophysiology of SVT
Thefour main typesof SVT are atrial fibrillation, paroxysmal SVT, atrial flutter, and Wolff–Parkinson–White (WPW) syndrome.
Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12).
Paroxysmal SVTdescribes a situation where SVT reoccurs and remits in the same patient over time. Types:
- “Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
- “Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
- “Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than thesinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.
SVTs are often seen in patients with no pre-existing heart disease. It is usuallybenign and is rarely seen in the peri-arrest setting, making most SVTs ‘unpleasant’, rather than ‘life-threatening’.
Signs of SVT
- Tachycardia and tachypnoea
- Adverse signs:
- Hypotension
- Pallor
- Cold and clammy
- Signs of pulmonary oedema
- Raised JVP
Symptoms of SVT
- Patients may be asymptomatic
- Palpitations
- Shortness of breath
- Chest pain
- Dizziness
- Adverse symptoms:
- Ischaemic chest pain
- Syncope
- Confusion
- Sweating
Adverse features of SVT
- Shock: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
- Syncope: transient loss of consciousness due to a global reduction in blood flow to the brain
- Myocardial ischaemia: typical ischaemic chest pain and/or evidence of myocardial ischaemia on 12-lead ECG
- Heart failure: pulmonary oedema and/or raised jugular venous pressure
Primary investigations for SVT
12-lead ECG: regular, narrow-complex tachycardia (QRS <0.12) with a rate of 151 to 250 beats per minute - it looks like a QRS complex followed immediately by a T wave, QRS complex, T wave etc
Other investigations for SVT
- TFTs:hyperthyroidism is a secondary cause of SVT
- U&Es and metabolic panel: particularly screen for hyperkalaemia and hypokalaemia, as well as hyper- and hypocalcaemia
Acute management of stable patients with SVT
- Continuous ECG monitoring
- Correct reversible causese.g. electrolyte abnormalities
- Stepwise approach:
- Valsalva manoeuvre: ask the patient to blow hard against resistance, for example into a plastic syringe.
- Carotid sinus massage: massage the carotid on one side gently with two fingers.
- AdenosineWorks by slowing cardiac conduction primarily though theAV node. It interrupts theAV node/accessory pathwayduring SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway.
- Verapamil(calcium channel blocker): alternative to adenosine
- Direct current cardioversion:may be required if the above treatment fails
Long term management for pateints with paroxysmal SVT
If recurrent episodes of SVT:
- Medication (beta blockers,calcium channel blockersoramiodarone)
- Radiofrequency ablation
Complications for SVT
- Syncope
- Congestive heart failure: chronic, recurrent SVT that is left untreated may weaken the heart and result in heart failure
- Life-threatening arrhythmias: rarely, SVT may degenerate into a life-threatening arrhythmia, such as ventricular tachycardia or ventricular fibrillation
- Sudden death: occurs very rarely and the risk is generally very low
Prognosis for SVT
The prognosis associated with SVT depends on the presence of any underlying structural heart disease.
Patients with a structurally normal heart have an excellent prognosis, whilst the risk of sudden death is generally very small in the absence of pre-excitation (WPW syndrome).
Recurrent paroxysmal SVT requires lifestyle modifications, including reducing stress and caffeine intake, as well as smoking cessation.
Define Ventricular tachycardia
Rapid ventricular beating that may result in inadequate ventricular filling
Pathophysiology of V tach
Ventricular tachycardia (VT) occurs due to rapid, recurrent ventricular depolarisation from a focus within the ventricles. This is commonly due to scarring of the ventricles following myocardial infarction.
VT is a life-threatening arrhythmia that may lead to loss of consciousness, loss of cardiac output and ultimately cardiac arrest.
Polymorphic VT:
Polymorphic VT is a particular type of VT that is due todepolarisation of multiple foci within the ventriclesleading to variable QRS complexes. It is usually secondary to myocardial ischaemia.
Torsades de pointes is a subtype of polymorphic VTthat is characterised by ventricular tachycardia that ‘twists’ around the isoelectric line. This subtype occurs secondary to aprolonged QT interval.
Clinical manifestations of V Tach
- Breathlessness
- Chest pain
- Palpitations
- Dizziness/ syncope
- Hypotension
- Cardiac arrest
Investigations for V tach
ECG: rapid, broad-complex tachycardia (QRS >120 ms)
Management for V tach
- Consider up to 3 synchronised shocks
- IV amiodarone infusion
- Beta blockers: for management of symptoms
Define V Fib
This involves very rapid irregular ventricular activation with no mechanical effect i.e. no cardiac output.
Ventricular fibrillation (VF) occurs when the ventricular muscle fibres contract independently.
Clinical manifestations of V Fib
Cardiac arrest:
- Pulselessness
- Unconsciousness
- Respiration ceases
Investigations for V Fib
Patient is likely to be unconscious!
- ECG: no QRS can be identified, ECG is completely disorganised
Management for V Fib
- Immediate DC cardioversion
Define Ven Ectopic
Ventricular ectopics are premature ventricular beats
Epidemiology of V ectopic
- They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions, especially post-MI
Pathophysiology of V ectopic
Premature ventricular beat caused by electrical discharges from outside the atria.
Following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory to the next sinus impulse - resulting in a missed beat.
Bigeminy: ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.
Clinical manifestations of V ectopic
- Palpitations: complaints of extra beats, missed beats or heavy beats
- Patients may feel faint or dizzy
Investigations for V ectopic
- ECG: individual random, abnormal, broad QRS complexes on a background of a normal ECG.
- Check bloods foranaemia,electrolyte disturbanceandthyroidabnormalities
Management for V ectopic
- Reassurance and no treatment in otherwise healthy people
- Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)
Complications for V ectopic
- If the ectopics are frequent then left ventricular dysfunction may develop
- Can provoke VF = fatal
Define Long QT syndrome
A prolonged QT interval is the ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction.
Epidemiology for Long QT
Approximately 1 in 2500-7000 people are affected by long QT syndrome
RF for Long QT
- Romano-Ward syndrome:thecommonest cause of congenital LQT syndrome due to inheritance of a single copy of the variant gene (most commonlyKCNQ1), resulting in LQT syndromewithoutdeafness (autosomal dominant)
- Jervell-Lange-Nielsen syndrome: due to inheritance of two copies of the variant gene, resulting in marked QT prolongation and sensorineural deafness (autosomal recessive)
- Electrolyte imbalances
- QT-prolonging drugs
Patho/Aet for Long QT
A normal corrected QT interval is<430 ms in malesand<450 ms in females.
However, in long QT syndrome, the ion channels involved in myocardial ventricular repolarisation are affected, resulting in aprolonged QT intervalon an ECG.
Long QT syndrome can either becongenitaloracquired.
Drugs that cause long QT syndrome most commonly do so byblocking potassium channels.
Signs of long QT
- Micrognathia
- Low-set ears
- Widely spaced eyes
Symptoms of long QT
- Syncope
- LQT1: exertional syncope, often swimming
- LQT2: syncope following emotional stress, arousal or exercise
- LQT3: syncope at night or at rest
- Dizziness
- Palpitations
- Dyspnoea
- Collapse or sudden cardiac death
Primary investigations for long QT
- ECG:to identify the presence of long QT syndrome (QTc >430 ms in males and >450 in females)
- Serum electrolytes:especially potassium, magnesium, and calcium
Other investigations for long QT
- Holter monitor: allows evaluation of the QT interval behaviour at night (when the patient is bradycardic), and during day-time activity (when the patient is tachycardic)
- Exercise tolerance test: especially useful in the diagnosis of LQT1
- Echocardiogram: helpful in ruling out structural or valvular pathology
- Genetic testing: useful if a positive family history is uncovered as it allows pinpointing of the channelopathy and subtype responsible
Management for long QT
- Conservative: avoid precipitating factors (e.g. stress and exercise), correct electrolyte imbalance, cease QT-prolonging medication
- Beta-blocker:
- Prevents ventricular tachyarrhythmias in long QT syndrome but doesnotshorten the QT interval
- Propanolol is most commonly used and sotalol must beavoided
- Implantable cardioverter-defibrillator (ICD)is indicated for the following patients:
- Previous cardiac arrest
- Recurrent syncope despite beta-blocker treatment
- Unable to tolerate beta-blockers
- High-risk patients with a QTc >500ms
Complications of long QT
- Torsade de pointes:polymorphic ventricular tachycardia (VT) secondary to genetic mutations that result in slow repolarisation and a predisposition to VT.Waiting a longer time for repolarisation (long QT) can result in random spontaneous depolarisation in some areas of heart myocytes. Depolarisation without proper repolarisation is called Torsade de pointes.Management: correct the cause & magnesium infusion
- Cardiac arrest and sudden death:secondary to VT degenerating into ventricular fibrillation (VF)
Prognosis for long QT
The prognosis of patients with long QT syndrome will be determined by the length of QT prolongation (the longer the interval, the greater the risk of a cardiac event), symptom presence and syncopal episode.
Pathophysiology of Wolff Parkinson White (WPW)
- Caused by congenital accessory conduction pathway between atria and ventricles. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.
- There are 2 types
- Type A: +ve delta wave in V1
- Type B: -ve delta wave in V1
Clinical manifestations of WPW
Supraventricular tachycardia: may be due to AVRT or pre-excited AF/ flutter
Investigations for WPW
ECG: short PR interval, slurred upstroke (delta wave) and wide QRS complex
Management for WPW
- Flecainide, propafenone, sotalol, or amiodarone
- Ablation of the accessory pathway
